The goals of this project are to identify factors that may lead to gastric acid hypersecretion in patients with peptic ulcer disease. Emphasis during the current year will be given to identification of factors that inhibit acid secretion, especially intestinal peptides distinct from those already characterized in extracts of porcine intestine. Studies will be done to determine if circulating somatostatin is likely to influence gastric acid secretion or gastrin release. Other studies will be carried out to determine if bombesin-like peptides are likely mediators of gastrin release and if duodenal ulcer subjects appear to have a defect in autoregulation of gastrin release in response to food when intragastric pH is maintained at a low level. Initial attempts will be made to produce monoclonal antibodies to gastrin in order to use such antibodies in blocking experiments to neutralize circulating gastrin and thereby to establish further the role of circulating gastrin in regulation of food-stimulated gastric acid secretion.